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Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [RNA-seq]

ABSTRACT: Explore the potential downstream signaling pathways that inhibit TGEV replication after knocking out TMEM41B by RNA-seq analysis.

ORGANISM(S): Sus scrofa

PROVIDER: GSE169095 | GEO | 2021/11/19

REPOSITORIES: GEO

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Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [PigGeCKO]

Project description:We use the a porcine genome-scale CRISPR/Cas9 knockout (PigGeCKO) library (Zhao et al., 2020) to identify key host factors facilitating TGEV infection in porcine cells.

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Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [Focused cell]

Project description:We use the Focused-library to identify key host factors facilitating TGEV infection in porcine cells.

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Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-11-19 | GSE169113 | GEO

Genome-scale CRISPR screen identifies TMEM41B as a multi-function host factor required for coronavirus replication.

Project description:Emerging coronaviruses (CoVs) pose a severe threat to human and animal health worldwide. To identify host factors required for CoV infection, we used α-CoV transmissible gastroenteritis virus (TGEV) as a model for genome-scale CRISPR knockout (KO) screening. Transmembrane protein 41B (TMEM41B) was found to be a bona fide host factor involved in infection by CoV and three additional virus families. We found that TMEM41B is critical for the internalization and early-stage replication of TGEV. Notably, our results also showed that cells lacking TMEM41B are unable to form the double-membrane vesicles necessary for TGEV replication, indicating that TMEM41B contributes to the formation of CoV replication organelles. Lastly, our data from a mouse infection model showed that the KO of this factor can strongly inhibit viral infection and delay the progression of a CoV disease. Our study revealed that targeting TMEM41B is a highly promising approach for the development of broad-spectrum anti-viral therapeutics.

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Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication

Project description:Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication

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Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [PigGeCKO]

Project description:Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [PigGeCKO]

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Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [RNA-seq]

Project description:Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [RNA-seq]

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Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [Focused cell]

Project description:Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [Focused cell]

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TMEM41B is a host factor required for the replication of diverse coronaviruses including SARS-CoV-2.

Project description:Antiviral therapeutics are a front-line defense against virally induced diseases. Because viruses frequently mutate to escape direct inhibition of viral proteins, there is interest in targeting the host proteins that the virus must co-opt to complete its replication cycle. However, a detailed understanding of the interactions between the virus and the host cell is necessary in order to facilitate development of host-directed therapeutics. As a first step, we performed a genome-wide loss of function screen using the alphacoronavirus HCoV-229E to better define the interactions between coronaviruses and host factors. We report the identification and validation of an ER-resident host protein, TMEM41B, as an essential host factor for not only HCoV-229E but also genetically distinct coronaviruses including the pandemic betacoronavirus SARS-CoV-2. We show that the protein is required at an early, but post-receptor engagement, stage of the viral lifecycle. Further, mechanistic studies revealed that although the protein was not enriched at replication complexes, it likely contributes to viral replication complex formation via mobilization of cholesterol and other lipids to facilitate host membrane expansion and curvature. Continued study of TMEM41B and the development of approaches to prevent its function may lead to broad spectrum anti-coronavirus therapeutics.

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Genome-wide CRISPR screen identifies TMEM41B as a gene required for autophagosome formation.

Project description:Macroautophagy is an intracellular degradation process that requires multiple autophagy-related (ATG) genes. In this study, we performed a genome-wide screen using the autophagic flux reporter GFP-LC3-RFP and identified TMEM41B as a novel ATG gene. TMEM41B is a multispanning membrane protein localized in the endoplasmic reticulum (ER). It has a conserved domain also found in vacuole membrane protein 1 (VMP1), another ER multispanning membrane protein essential for autophagy, yeast Tvp38, and the bacterial DedA family of putative half-transporters. Deletion of TMEM41B blocked the formation of autophagosomes at an early step, causing accumulation of ATG proteins and small vesicles but not elongating autophagosome-like structures. Furthermore, lipid droplets accumulated in TMEM41B-knockout (KO) cells. The phenotype of TMEM41B-KO cells resembled those of VMP1-KO cells. Indeed, TMEM41B and VMP1 formed a complex in vivo and in vitro, and overexpression of VMP1 restored autophagic flux in TMEM41B-KO cells. These results suggest that TMEM41B and VMP1 function together at an early step of autophagosome formation.

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